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3.
Cardiologia ; 38(12 Suppl 1): 233-7, 1993 Dec.
Article in Italian | MEDLINE | ID: mdl-8020022

ABSTRACT

Numerous studies have already recognized the importance of diastole in the pathogenesis of congestive heart failure. Non-invasive evaluations are based particularly on echo-Doppler, on radionuclide angiography and on cine-nuclear magnetic resonance: they have enabled an accurate evaluation of diastolic function and dysfunction, although invasive hemodynamic study maintains a gold standard position. All these methods of study have consented the identification of 3 basic components (anatomic and functional): active relaxation, passive elastic relaxation, atrial function. The Authors have identified the causes of diastolic failure with a particular attention to the various components of diastole. They have analyzed the implication of therapy on the basis of a clear understanding of the etiology, pathogenesis and pathophysiology of the underlying cardiac disease.


Subject(s)
Heart Failure/drug therapy , Diastole/physiology , Heart Failure/physiopathology , Humans , Ventricular Function, Left/physiology
4.
Cardiologia ; 34(12): 1013-9, 1989 Dec.
Article in Italian | MEDLINE | ID: mdl-2634477

ABSTRACT

We evaluated haemodynamic parameters in 13 patients suffering from chronic heart failure (CHF) in III and IV NYHA class. They were 10 males and 3 females, average age 57 +/- 11 years. Haemodynamic monitoring was made at basal condition and for 40 min after the administration of nicardipine (10 mg iv). We observed that mean arterial pressure and systemic vascular resistances (SVR) showed an important decrease (respectively -10.8%, p less than 0.001 and -22%, p less than 0.001); total pulmonary resistances (TPR) also decreased (-16.6%, p less than 0.001), while mean pulmonary pressure did not show significant reduction. Cardiac index increased with the highest value at the fifteenth minute (-11.7%, p less than 0.01). Pulmonary wedge pressure (PWP) did not show statistic variations, and heart rate too. Cardiac index (CI) did not rise in 3 patients with clinical worsening during the monitoring (patients non responders) (CI increase was less than 15%); while in 10 patients CI increased more than 15% (patients responders). Patients non responders did not show any decrease of TPR and only a transitory reduction of SVR; patients responders showed an important decrease of TPR, SVR, PWP. We observed that at baseline, the difference between the 2 groups was based on the value of TPR and PWP. We conclude that nicardipine is an efficient drug in patients affected by CHF without severe hemodynamic failure.


Subject(s)
Heart Failure/drug therapy , Hemodynamics/drug effects , Nicardipine/pharmacology , Aged , Drug Evaluation , Female , Heart Failure/physiopathology , Humans , Male , Middle Aged , Nicardipine/therapeutic use
5.
Clin Cardiol ; 10(8): 470-3, 1987 Aug.
Article in English | MEDLINE | ID: mdl-3113793

ABSTRACT

Two groups of patients with angina were studied: Group A, 9 patients not treated previously with nitroderivatives; Group B, 8 patients, treated with transdermally administered nitroderivatives for at least 4 weeks. Hemodynamic parameters did not differ significantly in these groups under baseline conditions; only systolic blood pressure was higher in Group B (165 +/- 16 mmHg) than in Group A (144 +/- 15 mmHg). Hemodynamic modifications produced by administering nitroglycerin transdermally in these patient groups were evaluated 100 min after the transdermal application. In Group A significant reduction of systolic (144 +/- 15 to 126 +/- 18 mmHg, p less than 0.01) and diastolic blood pressure (83.36 +/- 70.1 +/- 13 mmHg, p less than 0.05), mean right atrial pressure (4.8 +/- 2.1 to 3 +/- 1.7 mmHg, p less than 0.005), mean pulmonary arterial pressure (18.6 +/- 2.6 to 16.7 +/- 2.8 mmHg, p less than 0.01), and significant increase of heart rate (72 +/- 10 to 83.5 +/- 12.4 beats/min, p less than 0.005) were noted. In Group B we noted only a significant reduction in systolic (170 +/- 25 to 150.5 +/- 16 mmHg, p less than 0.05) and diastolic blood pressure (88.7 +/- 15.5 to 77.5 +/- 9.2 mmHg, p less than 0.05) without other modifications. We conclude that prolonged treatment with adequate doses of transdermal nitroglycerin causes the hemodynamic effects of the medication to dissipate from the venous tone and significant arteriodilative effect to persist.


Subject(s)
Angina Pectoris/drug therapy , Hemodynamics/drug effects , Nitroglycerin/therapeutic use , Administration, Cutaneous , Angina Pectoris/physiopathology , Female , Heart Failure , Humans , Male , Middle Aged , Nitroglycerin/administration & dosage , Time Factors
6.
Radiol Med ; 72(9): 632-6, 1986 Sep.
Article in Italian | MEDLINE | ID: mdl-3763965

ABSTRACT

The authors report their experience in fibrinolytic therapy with Urokinase in acute myocardial infarction. There were 3 groups of treatment: 100 patients with intracoronary fibrinolytic therapy; 77 patients with peripheral venous fibrinolytic administration; 31 patients with conventional therapy. The 3 groups underwent, between 21 and 28 days after the acute event, a coronarographic examination to evaluate the persistence of patency of the vessels involved in the myocardial infarction. The short term results show that the fibrinolytic therapy (with the limitations due to the hemorrhagic complications associated with the use of Urokinase), especially via intracoronary, is significantly more useful and reliable than conventional therapy, which appears unsatisfactory. Therapeutic failures are probably due to diffuse atherosclerosis of the vessel and/or to the old age of the thrombus.


Subject(s)
Angiography , Coronary Angiography , Fibrinolytic Agents/therapeutic use , Myocardial Infarction/drug therapy , Evaluation Studies as Topic , Female , Fibrinolytic Agents/administration & dosage , Follow-Up Studies , Heparin/administration & dosage , Heparin/therapeutic use , Humans , Male , Middle Aged , Myocardial Infarction/diagnostic imaging , Time Factors , Urokinase-Type Plasminogen Activator/administration & dosage , Urokinase-Type Plasminogen Activator/therapeutic use
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